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Published on: June 7, 2019
Kinase activity is not required for alphaCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses
Mohammad Reza Hojjati1, Geeske M van Woerden, William J Tyler
1Department of Neuroscience, Erasmus University Medical Center, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands.
Abstract:
Using targeted mouse mutants and pharmacologic inhibition of alphaCaMKII, we demonstrate that the alphaCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, alphaCaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that alphaCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.
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